Abstract
Introduction: Infarct growth has been shown to be a predictor of clinical outcome following ischemic stroke and has been used as a surrogate in reperfusion studies. There are no data whether the association of infarct growth and clinical outcome depends on stroke etiology. Furthermore, there is uncertainty on how to handle small volume infarcts with some studies excluding them from analyses. We studied the relationship between infarct growth and functional outcome in stroke patients with small volume infarcts for subgroups with small and non-small vessel etiologies. Methods: We studied 37 patients in the MRI substudy of the Efficacy of Nitric Oxide in Stroke (ENOS) trial with baseline infarct volumes of ≤5ml. None of the patients were treated with reperfusion strategies. Brain MRI was performed serially at baseline within 48 hours of onset, on days 7 and 90. Infarct growth was measured as the volume difference between final T2 and baseline DWI lesions. Good functional outcome was defined as day 90 modified Rankin score ≤2 and poor as >2. Results: Among the 26 patients with underlying small vessel etiology, there was no difference between those with good and poor outcomes in terms of absolute [median 0.0 (IQR -0.4 to 1.1) vs 0.1 (-0.7 to 0.2) mL, p=0.802] and relative infarct growth [median -3 (-27 to 81) vs 8 (-46 to 10) %, p=0.802]. However, in the 11 patients with etiologies other than small vessel disease, patients with good outcome had less absolute [median -0.9 (-1.6 to 0.7) vs 3.2 (0.2 to 9.1) mL, p=0.033] and relative infarct growth [median -59 (-81 to 9) vs 154 (35 to 292) %, p=0.019] compared to those with poor outcome. Discussion: In small volume strokes, infarct growth was not associated with functional outcome for small vessel stroke although there was a significant association for other stroke etiologies. This novel finding in this small sample should be confirmed in larger studies. Our findings are expected as small vessel stroke involves occlusion of penetrating arterioles which supply small, limited yet strategically important brain regions. Thus, while infarct growth may be a suitable surrogate for clinical outcomes for small volume infarcts due to non-small vessel disease, but it may not be for small vessel strokes.
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